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Related Experiment Videos

T cell receptor gene expression in autoimmune mice.

J D Mountz, K E Huppi, M F Seldin

    Journal of Immunology (Baltimore, Md. : 1950)
    |August 1, 1986
    PubMed
    Summary

    Autoimmunity in mice with lpr/lpr and gld/gld genotypes shows abnormal T cell expansion. These T cells share molecular similarities with immature thymocytes, influenced by background genes.

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    Area of Science:

    • Immunology
    • Molecular Biology
    • Genetics

    Background:

    • Autoimmunity in lpr/lpr and gld/gld mice involves lymphadenopathy and T cell expansion.
    • The molecular characteristics of these expanded T cells are not fully understood.

    Purpose of the Study:

    • To investigate T cell receptor (TcR) gene expression abnormalities in T cells from autoimmune mice.
    • To compare these abnormalities to immature thymocytes and explore genetic influences.

    Main Methods:

    • Analysis of TcR beta, TcR alpha, and TcR gamma transcript expression in lymph node T cells.
    • Examination of Thy-1 expression and c-myb expression.
    • Comparison across different mouse strains (AKR, MRL, C57BL/6) with lpr/lpr and gld/gld genotypes.

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    Main Results:

    • Expanded T cells in lpr/lpr and gld/gld mice show altered TcR beta and TcR alpha transcript levels.
    • TcR beta expression strongly correlates with c-myb expression, but not always.
    • Specific TcR beta transcripts indicating nonfunctional rearrangements predominate in AKR-lpr/lpr mice.
    • MRL-lpr/lpr mice exhibit TcR gamma transcript expression and age-related decreases in thymic TcR beta and c-myb.

    Conclusions:

    • Peripheral T cells in autoimmune mice display molecular similarities to immature thymocytes.
    • Background genes interact with lymphoproliferative genes to cause specific molecular and cellular abnormalities.
    • Findings highlight complex genetic interactions in autoimmune disease pathogenesis.